5-HT receptors exert differential effects on seizure-induced respiratory arrest in DBA/1 mice.

Both clinical and animal studies demonstrated that seizure-induced respiratory arrest (S-IRA) contributes importantly to sudden unexpected death in epilepsy (SUDEP). It has been shown that enhancing serotonin (5-HT) function relieves S-IRA in animal models of SUDEP, including DBA/1 mice. Direct activation of 5-HT3 and 5-HT4 receptors suppresses S-IRA in DBA/1 mice, indicating that these receptors are involved in S-IRA.

Repeated neonatal isoflurane exposure facilitated stress-related fear extinction impairment in male mice and was associated with ΔFosB accumulation in the basolateral amygdala and the hippocampal dentate gyrus.

Volatile anesthetics elicit neurodevelopmental toxicity in rodents and primates and lead to more exaggerated anxiety-like behavior in response to future stress. Anxiety and fear are closely correlated and maladaptive fear-associated learning is regarded as the core mechanism underlying anxiety-related disorders. However, little is known about the interaction between early-life anesthetic exposure and future stress and the accompanying effect on fear-associated learning.

A network meta-analysis of the long- and short-term efficacy of sleep medicines in adults and older adults.

Background: This study focuses on seven commonly used hypnotics to comprehensively analyze the effects of long- and short-term use on sleep outcomes among adults and older adults.

Methods: A network meta-analysis was performed. The insomnia medications were classified into seven categories: benzodiazepines, z-drugs, melatonin, H1-antagonists, orexin receptor antagonists (ORAs), antidepressants, and anticonvulsants.

PPAR γ Prevents Neuropathic Pain by Down-Regulating CX3CR1 and Attenuating M1 Activation of Microglia in the Spinal Cord of Rats Using a Sciatic Chronic Constriction Injury Model.

Background: Previous studies have proved that peripheral nerve injury is involved in the pathogenesis of neuropathic pain (NP). The peripheral nerve injury primes spinal M1 microglia phenotype and produces pro-inflammatory cytokines, which are responsible for neurotoxic and neuronal hyper-excitable outcomes. Spinal peroxisome proliferator-activated receptor gamma (PPAR γ) has been shown to play an anti-inflammatory role in the development of NP.

PDTC ameliorates neuropathic pain by inhibiting microglial activation via blockage of the TNFα-CX3CR1 pathway.

Previous studies have suggested that pyrrolidine dithiocarbamate (PDTC), a nuclear factor κB (NF-κB) inhibitor, play a role in deterring nerve injury-induced neuropathic pain (NP) The activation of NF-κB pathway may contribute to spinal microglial activation, CX3CR1 and tumor necrosis factor-alpha (TNF-a) up-regulation. The aim of this study was to clarify whether PDTC could inhibit the development of neuropathic pain via decreasing TNF-a-induced CX3CR1 up-regulation. Sprague-Dawley rats were randomly divided into sham group and NP group.

Association between the variability of cerebral oxygen saturation during cardiopulmonary bypass and delayed postoperative neurocognitive recovery in cardiac valve surgical patients: A pilot study.

Aims Of The Study: The association between regional cerebral oxygen saturation (rSO2) and postoperative cognitive decline is controversial. In this study, we investigated the association between the real variability of regional cerebral oxygen saturation during cardiopulmonary bypass (CPB) and postoperative delayed neurocognitive recovery in patients undergoing heart valve surgery.

Methods Used To Conduct The Study: A total of 71 patients who underwent cardiac valve surgery were enrolled in this study.

Sevoflurane inhibits cardiac function in pulmonary fibrosis mice through the TLR4 signaling pathway.

Pulmonary fibrosis is often concomitant with myocardial injury. We studied sevoflurane's effects on cardiac function and the expression of the TLR4/inducible nitric oxide synthase (iNOS) signaling pathway on a pulmonary fibrosis model. C57BL/6J wild-type (WT) and TLR4-deficient (TLR4) mice were randomly divided into a control group and a pulmonary fibrosis group.

Outcomes of Infant Cardiac Surgery for Congenital Heart Disease Concomitant With Persistent Pneumonia: A Retrospective Cohort Study.

Objectives: There is still controversy about whether an infant should have cardiac surgery concomitant with ongoing persistent pneumonia. This study analyzes the outcome of surgical treatment for infants with left-to-right shunt congenital heart disease accompanied with persistent pneumonia and discusses the perioperative management strategies for these cases.

Design: This is a retrospective cohort study.

Identification of lncRNA expression profiles and ceRNA analysis in the spinal cord of morphine-tolerant rats.

Morphine tolerance is a challenging clinical problem that limits the use of morphine in pain treatment, but the mechanisms of morphine tolerance remain unclear. Recent research indicates that long noncoding RNAs (lncRNAs) might be a novel and promising target in the pathogeneses of diseases. Therefore, we hypothesized that lncRNAs might play a role in the development of morphine tolerance.

Pioglitazone Confers Neuroprotection Against Ischemia-Induced Pyroptosis due to its Inhibitory Effects on HMGB-1/RAGE and Rac1/ROS Pathway by Activating PPAR-ɤ.

Background/aims: Recent researches highlighted the protective potential of pioglitazone, a PPAR-γ agonist, in the progression of cerebral ischemia-reperfusion injury. However, there has been no study on the application of pioglitazone in treating ischemic stroke through mechanisms involving pyroptosis.

Methods: The cerebral injury was established by middle cerebral artery occlusion (MCAO).

Enhanced recovery after surgery pathway for patients undergoing cardiac surgery: a randomized clinical trial.

Objectives: Enhanced recovery after surgery (ERAS) pathways have not been reported in cardiac surgery. The aim of this study was to evaluate the clinical effectiveness and safety profile of ERAS pathways compared with routine care for patients undergoing cardiac valvular surgery.

Methods: A randomized clinical trial was conducted between July 2015 and November 2016.

Suppression of HDAC2 in Spinal Cord Alleviates Mechanical Hyperalgesia and Restores KCC2 Expression in a Rat Model of Bone Cancer Pain.

Epigenetic modulation participates in the mechanism of multiple types of pathological pain, so targeting the involved regulators may be a promising strategy for pain treatment. Our previous research identified the analgesic effect of the histone deacetylase (HDAC) inhibitor trichostatin A (TSA) on mechanical hyperalgesia in a rat model of bone cancer pain (BCP) via restoration of μ-opioid receptor (MOR) expression. However, the specific types of HDACs contributing to BCP have not been explored.

[Perioperative safety of Tibetan children with congenital heart disease undergoing cardiac surgery and anesthesia in low-altitude area].

To observe the clinical parameters and short-term prognosis of Tibetan high-altitude area children with congenital heart disease undergoing surgery and anaesthesia in low-altitude area, and to investigate the perioperative safety of the treatment.
 Methods: From January, 2016 to December, 2016, 14 children with congenital heart disease who underwent surgery were assigned into 2 groups (n=7 each): the high-altitude area group (X group, children from Tibetan Autonomous Region) and the low-altitude area group (H group, children from Hunan Province). Echocardiography data, perioperative hemodynamic changes, postoperative recovery, complication and perioperative serum N terminal pro B type natriuretic peptide (NT-proBNP) levels were recorded.

Inhibition of Rac1 ameliorates neuronal oxidative stress damage via reducing Bcl-2/Rac1 complex formation in mitochondria through PI3K/Akt/mTOR pathway.

Although the neuroprotective effects of Rac1 inhibition have been reported in various cerebral ischemic models, the molecular mechanisms of action have not yet been fully elucidated. In this study, we investigated whether the inhibition of Rac1 provided neuroprotection in a diabetic rat model of focal cerebral ischemia and hyperglycemia-exposed PC-12 cells. Intracerebroventricular administration of lentivirus expressing the Rac1 small hairpin RNA (shRNA) and specific Rac1 inhibitor NSC23766 not only decreased the infarct volumes and improved neurologic deficits with a correlated significant activation of mitochondrial DNA specific proteins, such as OGG1 and POLG, but also elevated Bcl-2 S70 phosphorylation in mitochondria.

Etanercept decreases HMGB1 expression in dorsal root ganglion neuron cells in a rat chronic constriction injury model.

In the present study, we examined the effect of etanercept on high mobility group box 1 (HMGB1) expression in dorsal root ganglion (DRG) neuron cells in a rat model of chronic constriction injury (CCI) of the sciatic nerve, with the aim of exploring the molecular mechanism underlying the therapeutic effect of etanercept on sciatica-related nociception and the potential interaction between tumor necrosis factor-α (TNF-α) and HMGB1 in DRG neuron cells. A rat CCI model was employed and the animals were randomly assigned to seven groups (n=20/group): untreated, sham only, sham/saline, sham/etanercept, CCI only, CCI/saline and CCI/etanercept. Our results revealed that compared with the sham/saline and sham/etanercept groups, thermal hyperalgesia and mechanical hyperalgesia, as well as HMGB1 expression at both the mRNA and protein levels in the DRG neuron cells, were induced by CCI, and were significantly inhibited by etanercept.

Microinjection of HSV-1 amplicon vector-mediated human proenkephalin into the periaqueductal grey attenuates neuropathic pain in rats.

We investigated the antinociceptive effect of microinjection of HSV-1 amplicon vector-mediated human proenkephalin (hPPE) into the ventral periaqueductal grey (PAG) on neuropathic pain in rats. Male Sprague-Dawley rats with chronic constriction injury (CCI)-induced neuropathic pain were microinjected into the ventral PAG with normal saline (NS), pHSVIRES-lacZ (SHZ), or HSV-1 amplicon vector pHSVIRES-hPPE-lacZ (SHPZ), respectively. Pain thresholds in the SHPZ-treated rats were significantly higher at day 3, then reached peak at day 14 and lasted until day 35 after PAG administration, and these effects were reversed by naloxone.

Incidence and risk factors of intraoperative awareness during general anesthesia.

Objective: To investigate the incidence of awareness during general anesthesia and analyze the risk factors in anesthetic practice and patient populations.

Methods: A total of 2 300 patients who underwent general anesthesia were included. Perioperative data and anesthetic drugs were collected prospectively.

[Regulation of inflammatory pain by NF-κB and CX3CR1 at the spinal cord of rats].

Objective: To observe the effect of intrathecal injection of nuclear factor-κB (NF-κB) inhibitor of pyrrolidine dithiocarbamate (PDTC) on pain sensitivity thresholds and the expression of spinal cord CX3C chemokine receptor 1 (CX3CR1) in monoarthritis (MA) model in rats.

Methods: Forty-eight Sprague-Dawley rats were randomly divided into 4 groups (12 each) after successful intrathecal catheterization: (1) sham operation with physiological saline group (the sham group); (2) MA with normal saline group (the MA group); (3) 10 μL 100 μmol/L PDTC before MA (the PDTC pre-treatment group); (4)MA before 10 μL 100 μmol/L PDTC (the PDTC post-treatment group). Normal saline or PDTC was injected 5 d after the intrathecal catheterization.

Intrathecal infusion of pyrrolidine dithiocarbamate for the prevention and reversal of neuropathic pain in rats using a sciatic chronic constriction injury model.

Background And Objectives: Recent studies have suggested that nuclear factor κB (NF-κB) may play a role in mediating nerve injury-induced neuropathic pain. Here, we examined the effects of intrathecal pyrrolidine dithiocarbamate (PDTC), a NF-κB inhibitor, on the development of neuropathic pain, spinal microglial activation, and CX3CR1 expression induced by sciatic chronic constriction injury (CCI) model in rats.

Methods: Under chloral hydrate anesthesia, male Sprague-Dawley rats (300-350 g) fitted with intrathecal catheters underwent either sciatic CCI or sham surgery.

[Sevoflurane preconditioning induced delayed neuroprotection against focal cerebral ischemia in rats].

Objective: To investigate whether the reactive oxygen species (ROS) and mitochondrial ATP-sensitive potassium (mitoKATP) channels were involved in delayed neuroprotection induced by sevoflurane on tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) levels.

Methods: Eighty-four male SD rats weighing 250 approximately 280 g, undergoing thread embolism of the right middle cerebral artery occlusion (MCAO) to cause focal ischemia for 2 h and then undergoing 24 h reperfusion, were randomly divided into 7 groups (n=12, each): a sham group(S), an ischemia-reperfusion group (I/R), a sevoflurane preconditioning group (Sevo), a 2-mercaptopropionylglycine (ROS scavenger)+sevoflurane group (MPG+Sevo), a 5-hydroxydecanoate (a mitoK(ATP) blocker) + sevoflurane group (5-HD+Sevo), an MPG group, and a 5-HD group. The protein level of TNF-alpha and IL-1beta in the cerebral issue was detected by enzyme linked immunosorbent assay (ELISA) and the expression of mRNA was measured by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR).

[Bispectral index, cerebral state index and the predicted effect-site concentration at different clinical end-points during target-controlled infusion of propofol].

Objective: To examine the predicted effect-site concentration of propofol at two clinical end-points: loss of verbal contact (LVC) and loss of consciousness (LOC), and to explore the relationship between bispectral index (BIS) values, cerebral state index (CSI) values and the predicted effect-site concentration during the target-controlled infusion of propofol.

Methods: In 20 patients during the target-controlled infusion of propofol, the propofol infusion was set at an initial effect-site concentration of 0.5 mg/L, and increased by 0.

[Cerebral state index the in monitoring and evaluating the induction of anesthesia with target-controlled infusion of propofol in adults].

Objective: To evaluate the accuracy of cerebral state index (CSI) as an indicator of anesthesia depth in patients in the induction of anesthesia with target-controlled infusion of propofol.

Methods: Forty ASA (American Society of Anesthesiologists) I approximately II patients scheduled for an operation under general anesthesia were anesthetized with target-controlled infusion of propofol. Target plasma concentration was 0.